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Clinical Biochemistry: Manual For 4th Year Students of The Foreign Faculty
Clinical Biochemistry: Manual For 4th Year Students of The Foreign Faculty
POPECHITS
CLINICAL BIOCHEMISTRY
Manual for 4th year students of the foreign faculty
GRODNO 2010
Grodno 2010
2
Authors: ss. of the Department of Anesthesiology and Reanimatology with the course
of Clinical Biochemistry of EI Grodno State Medical University, cand. of
med. sciences S.V. Lelevich
ss. of the Department of Anesthesiology and Reanimatology with the course
of Clinical Biochemistry of EI Grodno State Medical University, T.V.
Popechits
NTENTS
Preface.5
Laboratory evaluation of acid-base balance
and blood gases ..6
Laboratory evaluation of water and electrolyte balance.16
Laboratory evaluation of protein metabolism..27
Enzyme tests.33
Laboratory evaluation of carbohydrate metabolism38
Tests.......44
Tests nswers60
Literature..72
PREFACE
Clinical biochemistry is a clinical and diagnostics subject, which aims to put
forward, improve and use standard diagnostic methods, to monitor disease
development and treatment by biochemical methods. Clinical biochemistry helps to
make diagnosis, choice of treatment and prophylactic methods easier.
Clinical biochemistry is one of the most important parts of laboratory
diagnostics together with laboratory haematology, immunology, clinical serology and
microbiology, clinical toxicology. It possesses the largest number of diagnostic tests
that help understand pathogenesis and etiology of different pathological processes.
Information, obtained by biochemical methods help to evaluate the development of
pathological process on molecular, cellular and organ level. It is essential for early
diagnosis of a disease and also assessment of its therapy efficacy.
Clinical biochemistry is evolving rapidly in our era. During the last ten years,
more than a hundred of new analytical methods have appeared, including DNAdiagnostics, determination of tumor markers, apoptosis tests. Biochemical tests are of
great importance in diagnosis of endocrine, gastrointestinal, heart and renal diseases as
well as in toxicology. Clinical biochemistry is closely linked to such theoretical
subjects as general and bioorganic chemistry, biochemistry, histology, normal and
pathological physiology, normal and pathological anatomy.
This manual provides useful information about modern principles of evaluation
of protein and carbohydrate metabolism, water and electrolyte balance, acid-base
balance and enzyme tests.
The information provided in this manual helps to come up with optimal schemes
and algorhythms of laboratory diagnostics of numerous pathological conditions
including their treatment efficacy monitoring.
Renal tubule
Capillary
H2CO3
Na+
H+ + HCO3-
H2CO3
C
CO2
+
H2O
CO2
+
H2O
Hydrogen ions excretion begins at the second stage when the whole bicarbonate
is reabsorbed.
HPO42- ion cant be reabsorbed from renal tubules because of charge, but it can
bind secreted hydrogen ions. Produced H2PO4- is excreted in urine, HCO3- - is
reabsorbed into the blood. H+ buffered by HPO42- accounts for the titratable acidity
(TA).
H2PO4-/ HPO42- is an ideal urinary buffer. This mechanism is able to decrease
urinary pH to 4,8 (compared with blood pH 7,4). When this level is achieved,
phosphate enters renal tubules as H2PO4- ion, which is not able to accept protons. This
states depletion of the phosphate buffer reserve and activation of renal
ammoniogenesis.
After depletion of the latter two mechanisms, the kidneys switch to ammonia
buffer (NH3/NH4+). The main source of ammonia is glutamine desamination. As NH3
has no charge, it moves freely across the tubular cell membrane and appears in the
urine, where it binds secreted proton to produce ammonium ions (NH4+). NH4+ cant
be reabsorbed because of its charge. This process is termed as ammoniogenesis.
Tab. 2. Main parameters for acid-base balance evaluation
Parameter
REFERENCE VALUES
(for arterial blood)
7,35-7,45
2
35-45 mm Hg
3
21-27 mmol/l
(base excess or deficit)
0 2,5 mmol/l
= NBB
actual buffer base
NBB normal buffer base (=7,4 ., 2= 40 ..., t =37)
Additional
Anion gap (G):
G = ([Na+] + [K+]) - ([Cl-] + [HCO3-]) (8-16 mmol/l)
Anion gap is a sum of anions that cant be measured directly in blood serum
(anions of organic and non-organic acids, proteins). G consists of phosphates,
sulfates, pyruvate, lactate, ketone bodies and others.
TYPE OF DISTURBANCE
Acidosis
Alkalosis
Respiratory
Metabolic
Mixed
Combined
Compensated
Subcompensated
Non-compensated
Primary disturbance
Compensation
Primary
[+]
disturbance
disturbance
Compensation
Metabolic
acidosis
[HCO3-]
pC O 2
Metabolic
alkalosis
[HCO3-]
pC O 2
Respiratory
acidosis
pC O 2
[HCO3-]
Respiratory
alkalosis
pC O 2
[HCO3-]
Here the main types of acid-base balance disturbances are described more in
details.
Respiratory Alkalosis
Respiratory alkalosis is defined as a pH greater than 7.45 with a pCO2 less than 35
mm Hg. Respiratory alkalosis appears if removal of CO2 is greater than it`s
production by tissues.
[HCO3]
= + lg ------------CO2 s
Acute Respiratory Alkalosis
CO2 ; [HCO3] normal or;
Chronic Respiratory Alkalosis
CO2 ; [HCO3] ; or normal
Any condition that causes hyperventilation can result in respiratory alkalosis.
These conditions include:
10
[HCO3]
= + lg ------------CO2 s
1.
2.
3.
4.
15
% of body weight
75-80%
60%
Newborns
Adults under 60
Adults >60
Male
Female
54%
46%
mmol/l
Anions
mmol/l
Sodium
Potassium
Calcium
Magnesium
135-145
3,5-5,2
2,12-2,6
0,8-1
Chloride
Bicarbonate
G
96-107
21-27
8-16
17
Decreased plasma volume leads to decreased renal blood flow and total sodium
charge. It results in stimulation of juxtaglomerular apparatus and high renin
secretion.
Renin converts angiotensinogen into angiotensin-I.
Angiotensin-I is subsequently cleaved to angiotensin-II by angiotensinconverting enzyme (ACE).
Angiotensin-II directly stimulates adrenal cortex to secrete aldosterone.
Increase in extracellular volume stimulates release of atrial natriuretic factor
(NF). It increases sodium excretion and excretion of an equivalent amount of water.
It also suppresses aldosterone synthesis.
Water metabolism regulation
Water is excreted from the organism mainly by kidneys, GIT, lungs and skin.
Water loss is compensated by water intake with food and beverages, and also some
water is derived from metabolic processes (nearly 300 ml daily). If water intake is
restricted, its excretion occurs mainly by kidneys and least through lungs and skin.
Water excretion by kidneys is regulated by antidiuretic hormone (ADH). It
stimulates water reabsorption in the distal part of the nephron (Fig.2).
Fig.2. Physiological response to water depletion
Lack of water
Osmolality of ECF
Stimulation of ADH
secretion
Stimulation of thirst
Water reabsorption
in kidneys
Water intake
able. 7. The main parameters for the assessment of water and electrolyte
metabolism
Parameter
Reference values
Erythrocytes
ale 4,0-5,0 1012/l
Female 3,7-4,7 1012/l
Total protein
65-85 g/l
Haemoglobin
ale 130-160 g/l
Female 120-140 g/l
Ht
ale 45-55 %
Female 37-47 %
+
Na
135-145 mmol/l
Plasma osmolality
275-295 mosm/kg
MCV
80-93 fl
MCH
27-31 pg
Disturbances of water and electrolyte metabolism
The main types of disturbances of water and electrolyte metabolism are
dehydration and hyperhydration.
Dehydration is a state of negative water balance.
Hyperhydration is a state of positive water balance.
Disturbances of water and electrolyte metabolism are divided into three groups
according to sodium concentration and osmolality:
Isotonic plasma osmolality - 275-295 mOsm/kg, [Na] - 135-145 mmol/l.
Sodium and water are lost in almost equivalent amount.
Hypotonic plasma osmolality <275 /, [Na]<135 mmol/l. Water loss or
retention is predominant.
Hypertonic plasma osmolality >295 /, [Na]>145 mmol/l. Sodium loss
or retention predominates.
Dehydration
The reasons of water deficiency are restricted water intake or increased water
loss. Restriction of water intake occurs rarely in clinical practice.
The main reasons of water loss are:
1. Diabetes insipidus
Central
Nephrogenous
19
2. Increased perspiration
3. Profuse diarrhoea
4. Hyperventilation
In these cases hypotonic fluid is lost from the body. Increase in plasma
osmolality causes intracellular water to move into the blood vessels, but it can not
compensate hyperosmolality completely. As such dehydration is partially compensated
by intracellular deposit, clinical signs will not be severe.
Central diabetes insipidus often occurs after neurosurgical operations and
craniocerebral traumas. The reason of this disease is injury of pituitary gland or
hypothalamus which is accompanied by decreased ADH secretion. These patients
develop polydipsia and polyuria without glucosuria.
Nephrogenous diabetes insipidus usually develops as a result of chronic renal
pathology. The reason of this pathology is low sensitivity of receptors to ADH in renal
tubules. Clinical features are the same as in central diabetes insipidus. However, after
ADH administration diuresis does not decrease.
Sodium deficiency
The reasons of sodium deficiency are increased sodium excretion or restricted
intake.
Causes of sodium deficiency:
1. Renal losses
ARF, polyuric stage
Diuretic intake
Mineralocorticoids deficiency
Osmotic diuresis (in diabetes mellitus)
2. Skin losses
Dermatitis
Burns
Cystic fibrosis
3.Intestinal losses
Vomiting
Diarrhoea
Intestinal obstruction
Sodium can be lost with hypo- and isotonic fluid. In both cases the volume of
extracellular fluid decreases. It leads to stimulation of volume receptors and
aldosterone secretion.
In the cases of sodium loss its serum concentration does not reflect the total
sodium level in organism, as the level depends on simultaneous water loss. If sodium
is lost with hypotonic fluid its plasma concentration will be high. If sodium loss is
combined with water retention, the level will be lower than normal. Loss of equivalent
amount of water and sodium does not influence its plasma concentration.
Diagnostic of sodium and water loss predominance is shown in the table 8.
20
N or
insignificant
N
In the case of excess water loss, the osmolality of ECF increases, which is based
on water molecules movement from the cells to the interstitial fluid and vessels. In this
case, the clinical features will be mild.
In clinical practice, the severity of dehydration of extracellular space is divided
into three degrees. (ble. 9).
able. 9. Clinical diagnosis of severity of dehydration (WHO)
Degree of severity of
% of weight loss
Clinical signs
dehydration
3-6
Thirst, dryness of skin,
I
tachycardia
6-9
Thirst, dryness of skin,
II
tachycardia, oliguria,
hypotension
III
More than 9
Hyperhydration
This type of disturbance is usually due to water retention. Clinical signs of water
intoxication present as a result of cerebral oedema. Risk of cerebral oedema appears if
sodium concentration in serum approaches 120 mmol/l.
Sodium excess
The reasons of sodium excess are decreased sodium excretion or excessive
intake.
Causes of decreased excretion:
1. Decreased glomerular filtration rate (ARF, CRF)
2. Increased tubular reabsorption (mineralocorticoids excess, Conn syndrome,
Cushing syndrome)
3. Secondary hyperaldosteronism
Congestive heart failure
21
Nephrotic syndrome
Liver cirrhosis with ascites
Stenosis of a.renalis
Decreased sodium excretion is the most frequent reason of sodium excess in the
organism. The main reason of secondary hyperaldosteronism is fluid accumulation in
the third compartment. It can be due to congestive heart failure, shock, sepsis,
nephrotic syndrome, ascites. It leads to increased aldosterone secretion by adrenal
cortex and sodium retention. As a result, plasma osmolality increases that stimulate
osmoreceptors and causes ADH secretion. It leads to hyponatraemia despite of sodium
excess in the organism. Treatment of such condition should be etiological.
22
Hyponatraemia
Naserum< 135 mmol /l
Serum osmolality
Normal
280-290mOsm/g
Low
< 280 msm/kg
High
> 290 msm/kg
Pseudohyponatremia:
hyperlipidemia
hyperproteinemia
Hypotonic
hyponatremia
Hypertonic
hyponatremia:
Hyperglycaemia.
> 20 mmol/l
Hypovolemia
Sodium in urine
< 20 mmol/l
edema
Isovolemia
Potassium in urine
SIADH
> 20 /
< 20 /
Diuretic therapy,
vomiting
Hypoaldosteroni
sm
Liver cirrhosis,
Nephrotic
syndrome,
Heart failure
Hypovolemia
Vomiting, diarrhoea,
perspiration
Isovolemia
Acute water
intoxication
23
Hypernatraemia
Naserum> 150 mmol /l
smurine/ sm serum
~1
<1
Diabetes
insipidus:
Central(<0,5)
Nephrogenous(<1, >0,5)
Hypovolaemia
>1
Vomiting, diarrhea,
hyperhydrosis
Hypervolaemia
infusion of hypertonic
solutions N3);
Nl or sea water intake
Hypoaldosteronism with
decreased water intake
24
Isovolaemia
inadequate water
intake;
febris;
thyrotoxicosis
oesophagal
obstruction;
Hypokalaemia
[]serum < 3,5 mmol/l
To be excluded:
1. diuretic therapy
2. Vomiting ,diarrhoea;
3. insulin, salbutamol therapy
[]urine
> 20 mmol/l
< 22 mmol/l
< 20 mmol/l
[HCO3-]
N or >24 mmol/l
< 22 mmol/l
N or >24 mmol/l
Acute diarrhoea
26
Chronic diarrhoea
High sensitivity to diuretics
Villous adenoma
Laxative abuse
Hyperkalaemia
[]serum> 5,2 mmol/l
Main reasons:
1. Pseudohyperkalaemia;
2. Acute renal failure;
3. Diabetes mellitus;
4. Drug therapy:
) potassium-sparing diuretics: spironolactone, amiloride;
)NSAIDs: indomethacin, ibuprofen;
)captopril, heparin.
[HCO3-]plasma
< 22 mmol/l
22-24 mmol/l
Anion gap
[creatinin-]plasma
> 16 mEq/l
8-16 mEq/l
Diabetic ketoacidosis
1.Endocrine disease:
Adrenal medulla failure;
Hyporeninaemic hypoaldosteronism;
Mineralocorticoid resistance;
Addison`s disease (primary hypoaldosteronism)
2.Extrarenal causes.
27
Functions
Transport of hormones,
bilirubin, fatty acids,
bile acids, drugs
Maintaining of osmotic
pressure
1-globulins
1-antitrypsine
-lipoprotein
Prothrombin
Transcortin
Acid glycoprotein
Thyroxin-binding globulin
Trypsin inhibitor
Transport of lipids
Coagulating factor
Cortisol transport
Progesterone transport
Thyroxin transport
2- globulins
Ceruloplasmin
Antithrombin III
Haptoglobin
Plasminogen
Retinol- binding protein
Vitamin-D- binding protein
Copper transport
Inhibitor of coagulation
Binding of haemoglobin
Plasmin precursor
Vitamin transport
Calciferol transport
- globulins
lipoprotein
Transferrin
Fibrinogen
Lipid transport
Transport of iron
Factor of coagulation
28
-reactive protein
- globulins
Ig , , G, E, D
Activation of complement
system
Immune protection
% of total protein
52-65
2-4,5
10-15
6-13
10-19
29
g/l
35-50
1-3
6-9
4-9
6-13
65-82
1.
2.
3.
4.
5.
CLASSIFICATION (APP):
Main reactants of acute phase, concentration increases 100-1000 times within
6-12 h:
-reactive protein(RP)
Amyloid protein
Moderate increase of concentration ( 2-5 times) within 24 h:
-acid glycoprotein
- Antitrypsin
Haptoglobin
Fibrinogen
Mild increase of concentration (by 20 - 60%) within 48 h
Ceruloplasmin
Complement system
Neutral reactants of acute phase
Immunoglobulins G, A and M
2 macroglobulin
"Negative" reactants of acute phase, concentration decreases within 12 - 18 h
Albumin
Transferrin
C- reactive protein (RP) is the most responsive of the acute phase proteins,
the most clinically significant.
Normal RP concentration is 0-10 mg/l
This protein was so named because of its ability to bind the C-polysaccharide of
the cell wall of Streptococcus pneumoniae
Increases in CRP can be much greater than the other proteins. It may increase
100 times in bacterial infections, tissue damage, burns, tumors, necrosis.
Increased levels usually appear within 24 to 48 hours after injury or infection,
sometimes earlier than clinical signs
Increase in CRP may give an additional band on electrophoresis between and
fractions, which can be mistaken for monoclonal protein
In the following cases CRP determination has maximal clinical significance:
33
ENZYME DIAGNOSTICS
Enzyme diagnostics is one of the branches of enzymology. It has two main
directions:
1) use of enzymes as reagents for determination of normal and pathological
components in serum, urine, gastric juice etc.
2) determination of enzyme activity in biological material with a diagnostic
purpose.
Serum enzymes are divided into 3 groups:
1. Cellular enzymes enter the blood from different organs. Their activity in
serum depends on enzyme content in organs, molecular weight, intracellular
localization, rate of elimination. Cellular enzymes are divided into non-specific
and organ specific.
2. Secretory enzymes are synthesized by cells, enter the bloodstream and fulfill
their specific functions in the circulatory system. These are enzymes of
coagulation system and fibrinolysis, choline esterase etc.
3. Excretory enzymes are synthesized by glands of GIT and enter the blood
(amylase, lipase).
Enzymes synthesis, functioning and breakdown take place continuously and
simultaneously; providing their given concentration and activity. Enzymes are
localized in different cellular compartments (cytoplasm, lysosomes, cellular
membrane, mitochondrions). That is why increased activity of certain enzymes can
indicate the degree of severity of cellular damage.
Here, we have provided information about enzymes which are most frequently used in
clinical practice for diagnosis, prognosis and therapy monitoring of different
pathologies. Their determination in blood serum has high clinical significance.
-amylase
High activity of this enzyme is observed in the liver, skeletal muscles,
microvillus of enterocytes, tears, secretion of mammary glands. Pancreas and salivary
glands are richest in amylase. Plasma contains two isoenzymes of -amylase:
pancreatic (P-type)- secreted by pancreas and salivary (S-type)- produced by salivary
glands. In norm pancreatic amylase constitutes 40 % of total serum amylase activity,
and salivary 60 %. Determination of -amylase activity is very important for
diagnosis of pancreatic pathology. Two times and more increased activity of -amylase
strongly indicates pancreatic damage.
In acute pancreatitis, -amylase activity in the blood and urine increases 10-30
times. Initial increase of -amylase activity is observed within 4-6 hours after the
beginning of the disease, reaches peak within 12-24 h; then decreases and returns to
norm within 2-6 days. Serum amylase level does not correlate with the degree of
severity of pancreatitis. Pathogenetically hyperamylasaemia appears when oedema of
interstitial tissue blokes the pancreatic ducts. It characterises fatty pancreatic necrosis.
In haemorrhagical pancreatic necrosis, rise in -amylase activity is observed in blood
with subsequent rapid decrease. This reflects progressing pancreatic necrosis.
34
Aminotransferases (L and S)
Aminotransferases catalyze the process of transamination, they are present in
every organ and tissue. Isoenzymes of AST are localized both in cytoplasm and in
mitochondrions. ALT predominates in cytoplasm. High concentration of AST is noted
in heart and skeletal muscles, liver, kidneys, pancreas and erythrocytes. Damage of any
of them leads to significant increase of AST in the blood serum. The most significant
increase of AST is observed in myocardial damage. In myocardial infarction, AST
activity in blood serum can increase 4-5 times. In acute myocardial infarction, 9398
% of patients have high AST activity; the latter has the same dynamic as Creatine
Kinase MB (CK-MB). However, CK-MB increase is more significant. Increase in AST
activity reveals hepatic pathology. The most significant increase is observed in acute
viral and toxic hepatitis. From mild to moderate increase in AST occurs in liver
cirrhosis (2-3 times), obstructive jaundice and liver metastasis. It can be also so in
skeletal muscular pathology, for example progressive muscular dystrophy; in
pancreatitis; intravascular haemolysis.
Low AST activity usually reveals vitamin 6 deficiency, renal failure,
pregnancy.
Highest concentration of ALT is noted in the liver cells. Skeletal muscles,
kidneys and heart also contain ALT, but much less. Increased ALT activity is most
frequently revealed in acute liver and biliary ducts diseases. ALT activity rises
significantly in the early stages of acute viral hepatitis: in 50% of patients ALT
increases 5 days before jaundice and hepatomegaly appear, in 90% of patients 2 days
before these symptoms. AST/ALT ratio is called de Ritis ratio. Its normal value 1
1,3. It decreases in liver diseases and increases in heart diseases. In toxic (alcoholic)
liver damage AST activity rises predominantly,where de Ritis ratio exceeds 2. In viral
hepatitis de Ritis ratio decreases. This ratio increases in obstructive jaundice,
cholecystitis, liver cirrhosis, while ALT and AST activity increase slightly.
Alkaline phosphatase (ALP)
The isoenzymes of alkaline phosphatase (ALP) are produced by various tissues:
intestinal mucous membrane, osteoblasts, biliary ducts, placenta, mammary gland
during lactation. This enzyme is situated on the cellular membrane and takes part in
transport of phosphorus.
Several isoenzymes of ALP are present in blood serum. Bone, liver and
placental ones are the most significant for clinical and diagnostic purposes.
1. Bone ALP. In bones ALP is secreted by osteoblasts. It is possible, that ALP
takes part in maturation of a bone matrix and its mineralization. ALP increases with
bone formation. Its significant increase in blood serum results from high osteoblastic
activity: growth of bones (children show higher ALP activity then adults; it also
increases in the last trimester of pregnancy), reactivation after prolonged
immobilization, fractures, deforming ostitis, rickets. It is also a characteristic for
osteomalacia (malignant bone tumors, multiple myeloma), tuberculosis of bones,
leukemia.
2. Liver ALP. There are two isoenzymes. The first one increases in blood serum in
biliary obstruction, due to decreased elimination of enzyme with bile. It also increases
35
in pregnancy (the second half). It is the main indicator of biliary tract pathology. The
second isoenzyme increases in hepatocellular pathology: viral hepatitis, liver cirrhosis.
But this increase is less significant in comparison to aminotransferases. 1/3 patients
with jaundice and liver cirrhosis show increase in ALP activity. Rise in ALP activity is
also revealed in 20% of patients with primary liver cancer or liver metastasis.
3. Intestinal ALP. It originates from enterocytes, enters the intestinal lumen and is
partially absorbed in the blood. It accounts for a small part of total ALP activity. Its
activity can be increased in people with I or III blood groups; especially after meals; in
intestinal diseases accompanied by diarrhoea.
4. Placental ALP. It normally appears in pregnancy. The highest activity is revealed
during the third trimester. It is the most thermostable isoenzyme of ALP. The most
significant increase develops in women with eclampsia as a result of placenta damage.
Low ALP activity in pregnancy indicates placental insufficiency.
Gamma-Glutamyl Transpeptidase (GGT)
The determination of GGT is of great significance in diagnosis of hepatic and
hepatobiliary pathology. This test is much more sensitive than either ALP or the
transaminase test in detecting obstructive jaundice, cholangitis, cholecystitis.
The highest GGT activity is noted in kidneys - 7000 times higher than in blood
serum. In healthy individuals serum GGT activity is low. The liver is considered as the
main source of normal serum activity, despite the fact that the kidney has the highest
level of the enzyme. Pancreas also contains GGT. Small enzyme concentration is
detected in intestine, brain, heart, spleen, prostate gland, skeletal muscles. GGT is
located in cellular membrane, lysosomes, cytoplasm. Membrane localization of GGT is
characteristic for cells with high secretory, excretory or reabsorptional activity. Serum
GGT activity increases in any pathology of liver and bile ducts. If GGT activity is
normal, liver disease probability is very low. Thus, GGT is good marker for
differential diagnosis of liver pathology. The most significant increase is observed in
cholestasis and slight increase - in parenchymal liver disease (necrosis of hepatocytes).
GGT activity rises on the early stage of the disease and remains high for a long time.
Beside this, GGT is a specific indicator of liver disease, because in comparison to ALP
its activity is normal in healthy children, pregnant women and patients with bone
diseases.
Determination of GGT activity is also used for diagnosis of alcoholic liver
disease and its therapy monitoring. Alcohol induces GGT synthesis in the liver and
release from cell membranes. It leads to increase of enzyme activity in the blood serum
without hepatic cell damage.
GGT test is also used for diagnosis of pancreatic pathology. Nowadays in
Europe, this parameter is used even more often than -amylase traditional indicator
of pancreatic pathology. 100% of patients with acute pancreatitis show GGT activity
10-20 times higher than normal.
This test can also be useful for laboratory diagnosis of renal pathology. It is
proven that GGT activity in urine rises significantly in pyelonephritis,
glomerulonephritis and renal calculi. Determination of GGT in urine allows to
36
diagnose the early stages of kidney disease, which is accompanied by proximal renal
tubular damage.
Creatine inase (C)
C is a dimer and consists of 2 protein subunits: (brain) and (muscle), which
combine to form 3 isoenzymes:
C- (C-1) brain
C- (C-2) cardiac
C- (C-3) muscle
38
Reactive hypoglycaemia
Fasting hypoglycaemia
Hypoglycaemia in DM
HYPOGLYCAEMIA
DIAGNOSIS
Acute: fatique and general malaise, hunger,
dizziness, vision disturbances and others.
Chronic (neurohypoglycaemia): psychosis,
amnesia, personality or behavioral changes
Clinical signs
Glucose administration
HYPERGLYCAEMIA
DIABETES MELLITUS
Diabetes mellitus (DM) it is a group of metabolic disorders, characterized by
hyperglycaemia due to insulin deficiency or defects in insulin action, or both of them
(WHO, 1999).
DM classification (WH, 1999):
Diabetes mellitus type 1
Other types of DM
Gestational DM
Appears in pregnancy
40
Before 30 years
After 40 years
Insulin deficiency
Absolute
Relative
Body weight
Overweight
Beginning of the
disease
Ketoacidosis
Acute
Insiduous
Often
Is not characteristic
Clinical course
Labile
Stable
1.
2.
3.
4.
Test procedure:
The patient fasts overnight. Water, but no other beverage, is allowed.
A venous sample is withdrawn for plasma glucose estimation.
75 g of glucose dissolved in 300 ml of water is given (for children 1,75 g/kg
body weight up to a maximum of 75 g). The patient must drink it within about 5
minutes.
Futher blood sample is taken at two hours after the glucose load
DEFINITIONS
Fasting glycaemia blood glucose level in the morning before breakfast after
overnight fasting > 8 h
Postprandial glycaemia blood glucose level two hours after meals
Glycemic profile blood glucose level determination every 3-4 hours during the
day
Random hyperglycaemia hyperglycaemia, revealed in any time of a day
PARAMETER
Glycemic self-control
HbA1c
Microalbuminuria
Haemogram, urinalysis,
biochemical blood tests
ESG, blood pressure
control
Feet examination
Consultation of
ophthalmologist,
neurologist, cardiologist
D MONITORING
FREQUENCY OF INVESTIGATION
DM TYPE I
In decompensation
every day
Once a 3 months
DM TYPE II
In decompensation every day
Twice a year
Once a 3 months
Once a year
42
< 4,8
4,8-6,0
> 6,0
CHOLESTEROL
OF HDLP
> 1,2
1,2-1,0
< 1,0
CHOLESTEROL
OF LDLP
< 3,0
3,0-4,0
> 4,0
AG
< 1,7
1,7-2,2
> 2,2
CMPLICATIONS OF DM
ARLY:
1. Diabetic ketoacidosis
2. Comas: ketoacidotic, lactacidotic, hyperosmolar non-ketotic, hypoglycaemic.
LATE:
1. Microangiopathy: neuropathy, nephropathy, retinopathy.
2. Macroangiopathy: coronary heart disease, cerebrovascular diseases, peripheral
angiopathy.
EARLY COMPLICATIONS OF DM
Diabetic ketoacidosis
The main reason bsolute insulin deficiency
Clinical signs
Diagnosis
Clinical signs of DM + smell of acetone in expired
air
Routine urinalysis
Glucosuria
Ketonuria
Hyperglycaemia
Hyperketonaemia
Acid-base status
Glycaemia
Acetone urine test
Therapy control
Once an hour until a level of 14 mmol/l is reached,
then once every 3 hours
Once a day
Initial
Initial
Acid-base status
Diuresis
Control hourly
Plasma osmolality
Diagnosis
Diabetes mellitus
clinical signs
Hyperglycaemia (> 50 mmol/l)
Absence of ketonaemia and acidosis
Hypernatraemia
Increased
Routine urinalysis
Glucosuria
Clinical signs
Biochemical blood analysis
LATE CMPLICATIONS OF DM
Diabetic nephropathy
Diabetic nephropathy (DN) specific renal blood vessels involvement in
diabetes mellitus that is accompanied by nodular or diffuse glomerulosclerosis.
Terminal stage of this process is characterized by development of chronic renal failure
(CRF).
STAGES:
Microalbuminuria
Proteinuria (> 0,5 g/24 h)
CRF
44
Tests
1. pH reflects:
1. Free hydrogen ions concentration.
2. Concentration of hydroxyl anions.
3. Hydrogen ions concentration to hydroxyl anions concentration ratio.
4. Hydrogen ions partial pressure.
2. Which buffer system predominated inside cells?
1. Bicarbonate
2. Acetate
3. Protein
4. Phosphate
5. Haemoglobin
3. pK of a bicarbonate buffer is:
1.7,3
2.7,4
3.6,1
4.5,9
5.7,8
4. Through which mechanisms do kidneys take part in regulation of acid-base
balance?
1. Maintaining of pCO2
2. Bicarbonate ions reabsorption
3. Hydrogen ions excretion
4. Bicarbonate ions regeneration
5. Nonvolatile acids formation
5. Which enzyme in renal tubules catalyzes dissociation of carbonic acid?
1. Lactate Dehydrogenase
2. AST
3. ALT
4. Lipase
5. Carbonic Anhydrase
6. Which anticoagulant is used for determination of parameters of acid-base
balance?
1. Oxalate
2. Citrate
3. Heparin Li
4. Heparin-Na
5. EDTA
45
7. What are the main organs taking part in regulation of acid-base balance?
1. Lungs
2. Kidneys
3. Liver
4. Spleen
5. Small intestine
8. Acidosis is characterized by:
1. Increased blood pH
2. Increasing of blood hydroxyl anions concentration
3. Decreased blood pH
4. Increased hydrogen ions concentration in the blood
5. Decreased lactate blood level
1. 50 mm Hg
2. 60 mm Hg
3. 70 mm Hg
4. 80 mm Hg
5. 100 mm Hg
14. Reference values of plasma bicarbonate concentration are:
1. 18-26 mmol/l
2. 21-27 mmol/l
3. 35-45 mmol/l
4. 25-30 mmol/l
5. 31-37 mmol/l
15. Reference values of arterial blood pH are:
1. 7,50-7,60
2. 7,35-7,60
3. 7,35-7,45
4. 7,25-7,45
5. 7,25-7,35
16. Life threatening bicarbonate ions concentration is above:
1. 35 mmol/l
2. 38 mmol/l
3 27 mmol/l
4 40 mmol/l
5. 29 mmol/l
17. Titrable acidity is:
1. Quantity of ammonium ions excreted in urine
2. Quantity of excreted phosphate anions
3. Quantity of excreted free hydrogen ions
4. Free hydrogen ions level in blood
18. Life threatening respiratory acidosis is characterized by:
1. pH less than 7,35
2. pCO2 is above 60 mm Hg
3. pCO2 is above 50 mm Hg
4. pH less than 7,20
5. pH less than 7,30
19. Life threatening respiratory alkalosis is characterized by:
1. pH less than 7,35
2. pCO2 less than 20 mm Hg
3. pCO2 less than 25 mm Hg
4. pH more than 7,60
47
1. 6 mmol/l
2. 5 mmol/l
3. 4 mmol/l
4. 3 mmol/l
5. 2,5 mmol/l
27. Parameter D(A-a)pO2 reflects:
1. Intrapulmonary shunting
2. Alveolar to arterial oxygen gradient
3. Partial pressure of oxygen in mixed venous blood
4. Partial pressure of oxygen in arterial blood
28. Parameter D(a-v)pO2 reflects:
1. Intrapulmonary shunting
2. Alveolar to arterial oxygen gradient
3. Arterial to venous oxygen gradient
4. Partial pressure of oxygen in arterial blood
29. pH=7,22; pCO2=61 mm Hg; bicarbonate=23 mmol/l; BE= -1,2 mmol/l. This
acid-base laboratory analysis is typical for:
1. Non-compensated metabolic acidosis
2. Non- compensated respiratory acidosis
3. Respiratory alkalosis and metabolic acidosis
4. Metabolic alkalosis and respiratory acidosis
30. pH=7,1; pCO2=66 mm Hg; bicarbonate=13 mmol/l; BE= -13 mmol/l. This
acid-base laboratory analysis is typical for:
1. Non-compensated metabolic acidosis
2. Non-compensated respiratory acidosis
3. Respiratory acidosis and metabolic acidosis
4. Metabolic alkalosis and respiratory acidosis
31. pH=7,55; pCO2=55 mm Hg; bicarbonate=45 mmol/l; BE= +15 mmol/l. This
acid-base laboratory analysis is typical for:
1. Subcompensated metabolic alkalosis
2. Non-compensated respiratory alkalosis
3. Respiratory alkalosis and metabolic acidosis
4. Metabolic alkalosis and respiratory acidosis
32. pH=7,41; pCO2=50 mm Hg; bicarbonate=30 mmol/l; BE= +7 mmol/l. This
acid-base laboratory analysis is typical for:
1. Compensated metabolic alkalosis
2. Compensated respiratory acidosis
3. Non-compensated metabolic acidosis
4. Non-compensated respiratory acidosis
49
2. 4,0-6,1 mmol/l
3. 5,6-7,8 mmol/l
4. 5,6-6,7 mmol/l
5. 7,8-10,0 mmol/l
40. Reference values of glucose in whole blood are:
1. 3,3-5,5 mmol/l
2. 3,9-6,4 mmol/l
3. 5,6-7,8 mmol/l
4. 5,6-6,7 mmol/l
5. 7,8-10,0 mmol/l
41. Hypoglycaemia can be caused by:
1. Adrenaline
2. Glucocorticoids
3. Insulin
4. Somatotrophin (growth hormone)
42. In suspected diabetes mellitus it is necessary to determine:
1. Blood glucose level
2. Urinary glucose
3. Glycosilated haemoglobin
4. Cholesterol
5. Triglycerides
43. Methods used for blood glucose determination:
1. Glucose oxidase method
2. Ortotolidine method
3. Hexokinase method
4. Biuret method
44. The true statements about glycosylated hemoglobin are:
1. Revealed in diabetes mellitus type II
2. Not founded in diabetes mellitus type I
3. Revealed in the blood of healthy people
4. Decreases in patients with diabetes mellitus
45. Fructosamine is:
1. Fructose connected with proteins
2. Mucopolysacharides
3. Glycosylated albumin
4. Glycolipids
46. Reference method for blood glucose level determination is:
1. Hexokinase method
51
2. Ortotolidine method
3. Benedicts test
4. Glucose oxidase method
5. Glucose dehydrogenase method
47. Postprandial glycaemia is:
1. Blood glucose level 1 hour after meals
2. Blood glucose level 6 hours after meals
3. Blood glucose level 3 hours after meals
4. Blood glucose level 2 hours after meals
48. Renal threshold for glucose is:
1. 6,0-7,0 mmol/l
2. 7,0-8,0 mmol/l
3. 8,8-10,0 mmol/l
4. 11,0-12,0 mmol/l
5. 12,0-13,0 mmol/l
49. Diagnostic criterion of diabetes mellitus is plasma glucose level in fasting
state:
1. >6,7 mmol/l
2. >5,6 mmol/l
3. >7,0 mmol/l
4. >5,5 mmol/l
5. >8,7 mmol/l
50. Diagnostic criterion of diabetes mellitus is whole blood glucose level in
fasting state:
1. >6,1 mmol/l
2. >5,6 mmol/l
3. >7,8 mmol/l
4. >5,5 mmol/l
5. >8,7 mmol/l
51. Diagnostic criterion of diabetes mellitus is plasma glucose level in 2 hours
after standard glucose load:
1. >6,4 mmol/l
2. >6,7 mmol/l
3. >7,0 mmol/l
4. >10,0 mmol/l
5. >11,1 mmol/l
52. Diagnostic criterion of diabetes mellitus is whole venous blood glucose level
in 2 hours after standard glucose load:
1. >6,4 mmol/l
52
2. >6,1 mmol/l
3. >7,8 mmol/l
4. >10,0 mmol/l
5. >11,1 mmol/l
53. Diagnostic criterion of diabetes mellitus is whole capillary blood glucose
level in 2 hours after standard glucose load:
1. >6,4 mmol/l
2. >6,7 mmol/l
3. >7,8 mmol/l
4. >10,0 mmol/l
5. >11,1 mmol/l
54. Glycosylated haemoglobin is:
1. Glucose combined with COHb
2. Glucose combined with HbA
3. Glucose combined with HbF
4. Fructose combined with HbA
55. Diagnostic significance of HbA1c :
1. Diagnosis of diabetic nephropathy
2. Estimation of hyperglycaemia duration
3. Diagnosis of diabetic ketoacidosis
4. Diagnosis of diabetic macroangiopathy
5. Diagnosis of diabetic retinopathy
56. One of the main laboratory criteria of diabetic nephropathy is:
1. Microalbuminuria
2. Proteinuria > 0,5 g/24h
3. Proteinuria > 1,0 g/24h
4. Proteinuria > 3,0 g/24h
5. Proteinuria > 2,0 g/24h
57. Microalbuminuria is:
1. Albumin excreted in urine in a quantity of 500-600 mg/24h
2. Albumin excreted in urine in a quantity of 600-800 mg/24h
3. Albumin excreted in urine in a quantity of 300-500 mg/24h
4. Albumin excreted in urine in a quantity of 30-300 mg/24h
58. Early complications of diabetes mellitus are:
1. Diabetic neuropathy
2. Diabetic nephropathy
3. Diabetic ketoacidosis
4. Diabetic retinopathy
5. Occlusion of femoral artery
53
1. <6,5 mmol/l
2. <6,2 mmol/l
3. <7,0 mmol/l
4. <5,2 mmol/l
5. <7,6 mmol/l
66. Main risk factors of developing atherosclerosis are:
1. High level of HDL and low level of LDL in serum
2. High level of LDL and low level of HDL in serum
3. Existence of modified lipoproteins
4. High level of chylomicrons
67. Steatorrhoea is:
1. Bile and gall stones formation
2. Fatty infiltration of the liver
3. Excess of fat in stools
4. Increased blood lipoproteins concentration
68. Which conditions should be maintained while laboratory investigation of
parameters of lipid metabolism?
1. Obtain blood from fasting patient
2. Use heparinised plasma for investigation
3. Use dry defatted tubes
4. Follow cholesterol-free diet 2-3 days before investigation
69. Screening tests for lipid exchange assessment include:
1. Total cholesterol
2. Phospholipids
3. Apolipoprotein A
4. Triglycerides
5. Fatty acids
70. What are the reasons of hypocholesterolaemia?
1. Nephrotic syndrome
2. Glomerulonephritis
3. Hard physical exercises
4. Insulin deficiency
5. Phaeochromocytoma
71. Which parameters should be determined in serum in order to identify the
type of hypolipoproteinaemia?
1. -cholesterol level
2. Total cholesterol
3. Main types of lipoproteins
4. LDL level
55
5. Triglycerides level
72. Apolipoproteins content may change in:
1. Coronary heart disease
2. Diabetes mellitus
3. Familial hyperlipidaemia
4. Pneumonia
73. Increased level of serum triglycerides may be revealed in:
1. Obesity
2. Alcoholism
3. Diabetes mellitus
4. Diabetes insipidus
74. In fasting serum from healthy individuals following types of lipoproteins
are revealed:
1. LDL
2. Cholesterol
3. Chylomicrons
4. VLDL
75. Hypertriglyceridaemia may develop in:
1. Pancreatitis
2. Diabetes mellitus
3. Hepatitis
4. Thyrotoxicosis
5. Starvation
76. Atherogenous effect is characteristic for:
1. LDL
2. VLDL
3. Phospholipids
4. Polyunsaturated fatty acids
5. HDL
77. Antiatherogenous effect is characteristic for:
1. Triglycerides
2. Cholesterol
3. Pre-- lipoproteins
4. - lipoproteins
5. - lipoproteins
78. Apolipoprotein is:
1. Protein that forms protein-lipid complex
2. Protein that determines properties of protein-lipid complex
56
3. 30-40 g/l
4. 60-80 g/l
92. Life threatening hypoalbuminaemia is:
1. Albumin level is less than 50 g/l
2. Albumin level is less than 45 g/l
3. Albumin level is less than 20 g/l
4. Albumin level is less than 30 g/l
93. Proteinuria is:
1. Protein excreted in the urine in a quantity above 20 mg/24h
2. Protein excreted in the urine in a quantity of more than 150 mg/24h
3. Protein excreted in the urine in a quantity of more than 50 mg/24h
4. Protein excreted in the urine in a quantity of more than 30 mg/24h
94. Dysproteinaemia is:
1. Increased concentration of total plasma protein
2. Decreased concentration of total plasma protein
3. Decreased fibrinogen level
4. Altered ratio of plasma proteins fractions
95. Decreased level of -globulins is observed in:
1. Coronary heart disease
2. Gastritis
3. Radiation sickness
4. Tumors of oesophagus
5. Rheumatoid arthritis
96. Bence-Jones protein can be revealed by:
1. Reaction of agglutination
2. Dialysis of the urine
3. Electrophoresis of the urine
4. Concentration of the urine
3. 6-8 g/l
4. 8-10 g/l
99. Increased level of fibrinogen is observed in:
1. Acute staphylococcus infections
2. Diabetes mellitus
3. Chronic hepatitis
4. Acute pancreatitis
5. Nephrotic syndrome
100.
Paraproteins can be revealed in:
1. Waldenstroms disease
2. Myeloma
3. Pneumonia
4. Light chain disease
101.
Transferrin is:
1. Globulin combined with magnesium
2. Globulin combined with iron
3. Globulin combined with sodium
4. Globulin combined with cobalt
5. Globulin combined with calcium
102. Which pathological states lead to hyperproteinaemia:
1. Increased synthesis of paraproteins
2. Hyperhydratation
3. Malabsorption of proteins in the intestine
4. Increased permeability of blood vessel wall
103. The main physiological function of haptoglobulin is:
1. Binding of haemoglobin
2. Acute phase protein
3. Takes part in immunological reactions
4. Takes part in blood coagulation
104. Inherited 1-antitrypsin deficiency leads to:
1. Emphysema in young people
2. Pyelonephritis
3. Hepatitis of newborns
4. Inflammatory and infectious lung diseases
105. Acute phase proteins are divided into:
1. Positive reactants
2. Active reactants
3. Negative reactants
60
4. Non-active reactants
5. Weakly active reactants
106. What are the main diagnostic purposes of CRP determination?
1. Diagnosis of neonatal sepsis
2. Differential diagnosis of viral and bacterial inflammation
3. Assessment of antibiotic therapy efficacy
4. Assessment of hyperglycaemia duration
107. Increasing of which acute phase protein is the most remarkable in
bacterial inflammation:
1. Haptoglobulin
2. Ceruloplasmin
3. CRP
4. Transferrin
5. Fibrinogen
108. The majority of enzymes reach maximal activity in the following range of
pH:
1. 1,5-2,0
2. 8,0-9,0
3. Nearly neutral
4. If pH=7,0 only
5. 5,5-6,5
109. Isoenzymes are:
1. Multiple forms of enzymes catalyzing different reactions
2. Multiple forms of enzymes catalyzing the same reaction
3. Multiple forms of enzymes with different physical and chemical properties
4. Multiple forms of enzymes with the same physical and chemical properties
110. Enzymes activity is determined in:
1. Blood serum
2. Leucoconcentrates
3. Biopsy material
4. CSF
111. Maximal activity of ALT is revealed in:
1. Lungs
2. Liver
3. Skeletal muscles
4. Kidneys
5. Pancreas
112. Maximal activity of Creatine Kinase is revealed in:
61
1. Heart muscle
2. Prostate gland
3. Spleen
4. Kidneys
5. Pancreas
113. Creatine Kinase has following isoenzymes:
1. Muscular
2. Brain
3. Lung
4. Heart
5. Liver
114. Increased activity of -Glutamyl Transpeptidase in serum is revealed in:
1. Prostatitis
2. Gastritis
3. Pancreatitis
4. Cholestasis
5. Glomerulonephritis
115. Myocardial injury is accompanied by increased activity of:
1. Lipase
2. ALT
3. -Glutamyl Transpeptidase
4. -Amylase
5. Heart isoenzyme of Creatine Kinase
116. Lactate Dehydrogenase molecule consists of such subunits:
1. B and M
2. H and M
3. B,M and H
4. B and H
5. B
117. How many isoenzymes does Lactate Dehydrogenase have:
1. 2
2. 3
3. 5
4. 10
118. Myocardium is rich in:
1. LDH-1
2. LDH-2
3. LDH-3
4. LDH-4
62
5. LDH-5
119. Acid Phosphatase activity increases in:
1. Prostatitis
2. Gastritis
3. Bronchitis
4. Meningitis
120. Patient complains of an onset of acute pain in the abdomen. Laboratory
investigation revealed increased -Amylase activity . Which diagnosis
should be suspected?
1. Acute pancreatitis
2. Acute viral hepatitis
3. Renal calculi
4. Myocardial infarction
5. Acute pleuritis
121. Amylase isoenzymes are located in:
1. Prostate gland
2. Myocardium
3. Pancreas
4. Lungs
5. Salivary glands
122. Patient complains of an onset of acute retrosternal pain. Laboratory
investigation revealed increased activity of serum Creatine Kinase.
Suspected diagnosis is:
1. Acute pancreatitis
2. Acute viral hepatitis
3. Renal calculi
4. Myocardial infarction
5. Acute pleuritis
123. Which enzyme activity grows in increased bone resorption?
1. Alkaline Phosphatase
2. Amino Trasferases
3. Catalase
4. Acid Phosphatase
5. Lactate Dehydrogenase
124. Determination of which enzyme activity is the most significant in
pancreatic injury?
1. Cholinesterase
2. -Amylase
3. Creatine Kinase
63
4. LDH
5. -Glutamyl Transpeptidase
125. Which enzyme is considered to be early marker of myocardial
infarction?
1. LDH-5
2. Cholinesterase
3. -Amylase
4. Creatine Kinase
5. Alkaline Phosphatase
126. Which enzyme activity grows mostly in prostate gland cancer?
1. -Amylase
2. Creatine Kinase
3. Alkaline Phosphatase
4. Acid Phosphatase
5. ALT
127. Which enzymes activity should be determined in serum in suspected toxic
hepatic injury?
1. Cholinesterase
2. LDH
3. Creatine Kinase
4. -Glutamyl Transpeptidase
5. Acid Phosphatase
128. Which enzymes activity will increase in skeletal muscles injury?
1. Creatine Kinase
2. -Amylase
3. LDH
4. Amino Trasferases
129. Increased activity of serum Creatine Kinase is revealed in:
1. Muscular traumas
2. Alcoholic intoxication
3. Muscular dystrophy
4. Pyelonephritis
130. Markers of cholestasis are:
1. Amino Trasferases
2. LDH and Creatine Kinase
3. Hystidase and Urokinase
4. -Glutamyl Transpeptidase and Alkaline Phosphatase
131. Which enzymes activity is increased in pancreatitis:
64
1. Urokinase
2. Acid Phosphatase
3. -Glutamyl Transpeptidase
4. Alkaline Phosphatase
5. -Amylase
132. Which enzyme activity should be determined in serum in suspected
chronic hepatitis?
1. ALT, AST, -Glutamyl Transpeptidase, Cholinesterase, Alkaline
Phosphatase
2. LDH and Creatine Kinase
3. Acid Phosphatase and Urokinase
4. Alkaline Phosphatase isoenzymes
133. De Ritis ratio is:
1. ALT to AST ratio
2. Alkaline Phosphatase to Lipase ratio
3. -Glutamyl Transpeptidase to ALT ratio
4. AST to ALT ratio
5. AST to Acid Phosphatase ratio
134. Acid Phosphatase activity increases in:
1. Tumors of prostate gland
2. Pancreatitis
3. Pregnancy
4. Bone metastatic injury
135. Isoenzymes LDH-1 and LDH-2 content is high in:
1. Heart
2. Skeletal muscles
3. Liver
4. Tumor cells
5. Pancreas
136. -Glutamyl Transpeptidase activity increases in:
1. Toxic hepatic injury
2. Myocardial infarction
3. Intra- and extrahepatic cholestasis
4. Acute pancreatitis
137. Increasing of which Creatine Kinase isoenzymes is specific for myocardial
infarction?
1. CK-MM
2. CK-MB
3. CK-BB
65
4. CK-CC
138. Increased activity of Alkaline Phosphatase bone isoenzyme is
characteristic for:
1. Hepatic cirrhosis
2. Primary and secondary hepatic tumors
3. Intrahepatic cholestasis
4. Pagets disease
139. Water distribution in the organism depends on:
1. Osmotic pressure
2. Oncotic pressure
3. Blood cholesterol level
4. Permeability of blood vessel wall
140. Normal plasma osmolality is:
1. 140-180 mosmol/kg
2. 275-295 mosmol/kg
3. 350-385 mosmol/kg
4. 550-600 mosmol/kg
5. 600-650 mosmol/kg
141. Osmotic gap is increased in:
1. Ethanol intoxication
2. Hydrocyanic acid intoxication
3. Lead poisoning
4. Mercury intoxication
142. In norm osmotic gap does not exceed:
1. 10 mosmol/kg
2. 20 mosmol/kg
3. 30 mosmol/kg
4. 40 mosmol/kg
143. Reference values of plasma sodium are:
1. 120-130 mmol/l
2. 130-147 mmol/l
3. 135-148 mmol/l
4. 145-155 mmol/l
144. Life threatening hyponatraemia is:
1. <125 mmol/l
2. <130 mmol/l
3. <122 mmol/l
4. <120 mmol/l
66
70
Answers
1. 1
2. 5
3. 3
4. 2,3,4
5. 5
6. 3
7. 1,2
8. 3,4
9. 4,5
10. 3
11. 3
12. 1
13. 2
14. 2
15. 3
16. 4
17. 2
18. 2,4
19. 2,4
20. 1,3
21. 1,2
22. 2
23. 2
24. 3
25. 3
26. 1
27. 2
28. 3
29. 2
30. 3
31. 1
32. 1
33. 1
34. 4
35. 2
36. 2
37. 1
38. 2
39. 2
40. 1
41. 3
42. 1
43. 1,2,3
44. 1,3
45. 3
46. 1
47. 4
48. 3
49. 3
50. 1
51. 5
52. 4
53. 5
54. 2
55. 2
56. 2
57. 4
58. 3
59. 2
60. 1
61. 4
62. 4
63. 1
64. 1,2,4
65. 4
66. 2,3
67. 3
68. 1
69. 1,4
70. 3
71. 3
72. 1,2,3
73. 1,2,3
74. 1,3,4
75. 2
76. 1,2
77. 5
78. 1,2,3
79. 3
80. 3
81. 5
82. 4
83. 1
84. 1
85. 1
86. 4
71
87. 1,3,4
88. 3
89. 1
90. 1,2,4,5
91. 2
92. 3
93. 2
94. 4
95. 3
96. 3
97. 2
98. 1
99. 1
100.
1,2,4
101.
2
102.
1
103.
1
104.
1,3,4
105.
1,3
106.
1,2,3
107.
3
108.
3
109.
2,3
110.
1
111.
2
112.
1
113.
1,2,4
114.
4
115.
5
116.
2
117.
3
118.
1
119.
1
120.
1
121.
3,5
122.
4
123.
4
124.
2
125.
4
126.
4
127.
4
128.
1,3,4
129.
1,2,3
130.
131.
132.
133.
134.
135.
136.
137.
138.
139.
140.
141.
142.
143.
4
5
1
4
1
1
1,3,4
2
4
1,2,4
2
1
1
3
144.
145.
146.
147.
148.
149.
150.
151.
152.
153.
154.
155.
156.
157.
4
4
2,3,4
1
1
1,3,4
3
4
3
1,2,3
1,2,3
1
2,3,4
1
72
158.
159.
160.
161.
162.
163.
164.
165.
166.
167.
168.
169.
170.
5
1
3
1,3,4
2
3
1
2
2,3,4
1
2,3,4
4
5
Literature
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Stepanova, L.I. Alehnovich, V.S. myshnikov. n.: BelP, 2008.
2. Alan, H. Gowenlock Practical clinical biochemistry, sixth edition / Gowenlock H.
Alan CBC: New Delhi, India, 2002.
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faculty / S.V. Lelevich. Grodno: GSMU, 2007.
4. myshnikov, V.S. Methods of clinical laboratory investigations / V.S.
myshnikov, .: Dpress-inform, 2009.
5. myshnikov, V.S. Manual of clinical biochemical laboratory diagnostics / V.S.
myshnikov, n.: Belarus, 2000. In 2 vol.
6. Laboratory diagnostics of carbohydrate metabolism disturbances. Metabolic
syndrome, diabetes mellitus / V.V. Dolgov, .V. Selivanov and authors. .,
2006.
7. rshall, V. J. Clinical biochemistry / V. J. rshall, SPb.: Nevski dialect, 1999.
8. enshikov V.V. Manual of clinical laboratory diagnostics / V.V. enshikov .:
edicine, 1982.
9. kachuk V.A. Clinical biochemistry / V.A.kachuk. .: GOETAR-MED, 2004.
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Zylva, P.R.Pannal, ., 1988.
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